- Title
- Epithelial mesenchymal transition in respiratory disease: fact or fiction
- Creator
- Knight, Darryl A.; Grainge, Christopher L.; Stick, Stephen M.; Kicic, Anthony; Schuliga, Michael
- Relation
- NHMRC.1099569 http://purl.org/au-research/grants/nhmrc/1099569
- Relation
- Chest Vol. 157, Issue 6, p. 1591-1596
- Publisher Link
- http://dx.doi.org/10.1016/j.chest.2019.12.014
- Publisher
- American College of Chest Physicians
- Resource Type
- journal article
- Date
- 2020
- Description
- Aberrant wound repair and fibrosis play a fundamental role in many major diseases concerning pulmonologists, including all forms of pulmonary fibrosis as well as COPD, asthma, cystic fibrosis (CF), bronchiolitis obliterans syndrome (BOS), and bronchiectasis. Accordingly, understanding normal and abnormal wound repair in the lung is a major objective of many academic groups and industry programs; one aspect of wound repair requiring urgent attention focuses on what drives the increased number of extracellular matrix (ECM)-secreting mesenchymal cells. Several different sources/pathways have been offered to account for the increased pool of (myo)fibroblasts. De-differentiation of airway smooth muscle cells and migration toward the basal lamina has been proposed,1 as have pericytes2 and endothelial-mesenchymal transition.3,4 However, the most studied mechanism is epithelial-mesenchymal transition (EMT), in which epithelial cells lose epithelial characteristics and become more mesenchymal, gaining mobility and enhanced ability to secrete ECM. This highly dynamic process has been subcategorized according to the three main functions it is associated with: embryonic development (type I), wound healing and tissue repair (type II), and cancer (type III). In this translational review, the mechanisms, roles, and impact of EMT (particularly type II) in chronic lung diseases are discussed. We also evaluate whether current medications influence EMT and how we may affect this process in the future.
- Subject
- asthma; cell differentiation; COPD; fibrosis; wound repair; SDG 3; SDG 7; Sustainable Development Goals
- Identifier
- http://hdl.handle.net/1959.13/1432239
- Identifier
- uon:39031
- Identifier
- ISSN:1931-3543
- Language
- eng
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